When scuba diving, you use a mixture of gases with which we can breathe underwater. Oxygen is vital for man, but it can become toxic from a certain partial pressure, and other types of factors such as the time of exhibition.
Oxygen poisoning
The partial pressure (Pp) of a gas that is part of a mixture is the result of multiplying its concentration (%) by the absolute pressure to which it is subjected. . The values of partial pressure of oxygen (Pp O2) that can be supported for a given time without immediate or delayed alterations appearing, are shared between the limits of 0.17 to 1.7 ATA.
- If Pp O2 < 0.17 Atm, hypoxic syncope (loss of consciousness) may occur.
- If Pp O2 is between 0.4 and 1.7 Atm, hyperoxic pulmonary accidents may occur
- If Pp O2 > 1.7 Atm, neurological convulsive accidents may occur.
The causes of oxygen poisoning in immersion are produced bybreathing pure O2 under pressure (rebreather with closed circuit below 7 meters), or compressed air from 72 meters deep. p>
Clinical picture
Neurotoxicity
An initial phase usually appears with general malaise, nausea, tics of the facial muscles, muscle cramps, tachycardia, subsequently appearing a picture of epileptiform seizures type "Grand mal" (epileptic attack). The crisis is spectacular and dangerous, and trauma may appear if one is in a hyperbaric chamber, or pulmonary overpressure and drowning if it appears during immersion.
If the subject is removed from the hyperoxic environment, it is cured without sequelae, but if it persists in said environment, the number of crises will increase, so that it can trigger death.
- Prevention: Do not descend with compressed air below depths of 80 meters. If using nitrox, calculate the Pp of O2 according to the percentage of the mixture to know the maximum depth that we can reach with that mixture.
- Treatment: remove to the affected subject from the hyperoxic environment (ascend in immersion or reduce the pressure inside the hyperbaric chamber).
The medical staff will treat the patient as having a "Grand Mal" seizure (epileptic seizure).
Pneumotoxicity (lung irritation)
It is a slow and progressive effect dependent on the Pp O2 value that is established depending on the time we remain in that environment and is manifested by: cough, expectoration, respiratory difficulty, chest pain located behind of the sternum, decreased vital capacity, and alveolar edema (pulmonary flooding) may appear at the lung level.
It is very rare that it occurs in a recreational diver, since at least ten hours are necessary at six meters deep breathing pure O2 for the first signs to appear.
Carbon monoxide poisoning
It is a relatively common clinical condition in everyday life caused by the inhalation of gases resulting from the incomplete combustion of carbon (braziers, exhaust pipes, smoke from fires, etc.).
In underwater activities, the problem appears when the diver breathes air contaminated with CO, which at ambient pressure is not toxic (25 parts per million of CO), but that same air breathed at a depth of 30 meters willcontain 100 ppm of CO, so it is already toxic. It is an odorless, colorless and tasteless gas, very difficult to detect when breathing the mixture in our bottle.
Pathophysiology
CO has up to 240 times more affinity for hemoglobin (protein that transports oxygen vital for cellular metabolism) than O2, and 40 times more affinity for myoglobin (protein that transports it at the muscle level), and produces >alteration at the level of cellular respiration.
Symptoms
Acute form
It presents mainly neurological symptoms, headache, nausea, vomiting, visual and auditory hallucinations, respiratory difficulty and obtundation. Pyramidal and extrapyramidal signs may appear (tremors, uncontrolled movements) and the appearance of erythematous plaques (red spots) and redness of the skin is common. the face. In severe poisoning, loss of consciousness.
Cardiac alterations with arrhythmias and changes in the EKG (ST alterations and flattening or inversion of the T wave), and pulmonary alterations, such as Acute lung edema, are part of CO poisoning. After the initial phase, a late and irreversible neurological demyelinating syndrome (deterioration of nerve conductions) may appear.
Chronic form
It is characterized by headaches, loss of appetite, insomnia, irritability, facial paresis (tingling), dizziness, and anemia. Its diagnosis will be based mainly on the clinical history complemented by the determination of carboxyhemoglobin levels in plasma.
Prevention and treatment
Use appropriate lubricants and filters in the load compressor, and avoid sources of CO in the compressor air intake (example: car exhaust fumes). Out-of-hospital treatment: oxygen at the highest possible concentration. At the hospital level, administer oxygen therapy in a hyperbaric chamber in order to:
- Increase dissolved O2, correcting tissue anoxia (lack of O2 in the tissues) immediately.
- It promotes the separation of hemoglobin from carbon monoxide (carboxyhemoglobin) and its transformation into oxygenated hemoglobin (oxyhemoglobin).
- Avoid late neurological sequelae.
Recommended regimen: 46 minutes at 3 ATA and subsequently decompressing for 30-60 minutes. In most cases a spectacular response is obtained within the first 30 minutes.
In severe poisonings it is advisable to repeat the sessions an hour later to displace the CO fixed at the intratissue level and, subsequently, perform two to five sessions of 45 minutes at 3 ATA during the first 48 hours to prevent appearance of late neurological demyelinating syndrome.
It is not a rare clinical condition, but it could justify many fatal accidents of unclear causes in divers who dive at deep levels.
Carbon dioxide poisoning
Carbon dioxide is a colorless gas, somewhat denser than air, which is in face. In severe poisoning, loss of consciousness.
Cardiac alterations with arrhythmias and changes in the EKG (ST alterations and flattening or inversion of the T wave), and pulmonary alterations, such as Acute lung edema, are part of CO poisoning. After the initial phase, a late and irreversible neurological demyelinating syndrome (deterioration of nerve conductions) may appear.
Chronic form
It is characterized by headaches, loss of appetite, insomnia, irritability, facial paresis (tingling), dizziness, and anemia. Its diagnosis will be based mainly on the clinical history complemented by the determination of carboxyhemoglobin levels in plasma.
Prevention and treatment
Use appropriate lubricants and filters in the load compressor, and avoid sources of CO in the compressor air intake (example: car exhaust fumes). Out-of-hospital treatment: oxygen at the highest possible concentration. At the hospital level, administer oxygen therapy in a hyperbaric chamber in order to:
- Increase dissolved O2, correcting tissue anoxia (lack of O2 in the tissues) immediately.
- It promotes the separation of hemoglobin from carbon monoxide (carboxyhemoglobin) and its transformation into oxygenated hemoglobin (oxyhemoglobin).
- Avoid late neurological sequelae.
Recommended regimen: 46 minutes at 3 ATA and subsequently decompressing for 30-60 minutes. In most cases a spectacular response is obtained within the first 30 minutes.
In severe poisonings it is advisable to repeat the sessions an hour later to displace the CO fixed at the intratissue level and, subsequently, perform two to five sessions of 45 minutes at 3 ATA during the first 48 hours to prevent appearance of late neurological demyelinating syndrome.
It is not a rare clinical condition, but it could justify many fatal accidents of unclear causes in divers who dive at deep levels.
Carbon dioxide poisoning
Carbon dioxide is a colorless gas, somewhat denser than air, which is in
